When we eat at regular intervals, our body is discouraged from storing calories. This statement is up for debate and there are certain factors we must take into account when considering the above.
In order to answer this question, we must look at our basal metabolic rate or BMR. BMR is the amount of energy released by our body when it is at rest. A high BMR means we can eat more food without getting fat. Exercise also plays a part in increasing our body’s BMR. However, there is no clear answer as to how often we should eat during a day. In a nutshell, eating several small meals a day is tied to the amount of energy our body needs to spend and not the quantity of mealtimes.[1]
Mealtimes in the western population are rapidly shifting towards a less structured pattern. With the rise in ready made meals and fast food chains, people have quick and easy access to food. Therefore, they are able to eat food at their own convenience, at any time or place. According to a study conducted on the subject, researchers have discovered that lacking consistency when it comes to eating may have negative effects on insulin.[2][3] An irregular eating pattern was linked to a decrease in what is known as thermic effect of food (TEF). This means that the body burns calories at a slow rate. It also leads to high concentrations of insulin in the blood. TEF triggers a signal in the brain indicating that the body is full and is no longer hungry. It is low in people who do not have fixed meal times, so an increase in their body weight occurs as a result.[4]
Free and multiple access VS. restricted access meals
Eating meals on irregular basis and lacking consistency is a potentially serious novel environmental risk factor.[2] This risk factor can lead to obesity and metabolic syndrome which includes increased blood pressure, high blood sugar and cholesterol. Stress is also a factor that should be taken into consideration. High levels of stress are capable of changing a person’s eating pattern and encouraging the consumption of tasty, highly palatable foods. In addition, there is rising evidence that irregular eating patterns can have negative effects on a person’s metabolism, especially in the absence of regular exercise. This adds credibility to the theory that highlights the advantages of staying consistent when it comes to eating several meals a day.[1][3]
Eating three meals per day, in addition to snacks, is the most common eating pattern in modern societies. However, this is considered abnormal from an evolutionary point of view.[5] Studies conducted on animal models and human subjects indicate that regular fasting which lasts up to sixteen hours can improve health and help combat diseases. It also encourages the body to shield from and repair damage on a cellular level.[6] However the data on intermittent fasting is yet sparse and all the mechanisms are not fully known. It means that to achieve the positive health outcomes fasting should be properly controlled for every individual. Until substantial research is done it is not recommended to include intermittent fasting as a part of weekly eating regime.[7]
Mice who were subjected to alternate day fasting diet while keeping the overall food intake unchanged remained the same weight-wise.[6] This intermittent fasting generated positive outcomes that surpassed those of the calorie restriction diet. These included low blood sugar and insulin levels in addition to better resistance of brain neurons to damage and death.[6]
A similar study also showed that mice who were subjected to time restricted feeding (TRF) received the same calories from their high food diet as those who were free to eat whenever they chose to.[8] Time restricted feeding means being fed within a specific window of time. The mice in the time restricted feeding group had protection against obesity and excessive insulin levels in the blood. They were also shielded from fatty liver when fat accumulates in the liver, leading to inflammation and liver failure. The TRF diet is mainly used as a non-pharmacological method to fight obesity and other diseases.[8]
Hunger and Satiety
When it comes to hunger and satiety, multiple studies have shown that more frequent meals per day may contribute to better appetite control.[9] While another review article agrees with it, the authors also report that eating 3 meals per day is associated with insignificantly lower calories intake when compared to more frequent meals.[10] Low frequency diet could be used for some specific groups of people requiring hypoenergetic (low energy) diet. It was found that eating breakfast and lunch is more effective than eating six smaller portions in low energy diets for type-2 diabetes patients.[11]
The question of timing is also very important when it comes to eating. This question has prompted researchers to look into the correlation of eating breakfast and evening meals to the total calories intake. They have shown that satiating morning meals and smaller evening meals reduce the daily calories intake and help people lose weight.[12][13]
Physical Exercise is Essential
In the absence of physical activity, eating multiple meals may not lead to better appetite control. It also does not change the body’s composition in a positive manner, especially in non-active people. Adequate protein levels may help athletic people in maintaining their lean body mass if they increase their number of meals. More meals than fewer have a positive effect on different blood markers of health such as LDL cholesterol, total cholesterol as well as insulin. It also helps decrease hunger and improve appetite control.[5]
A small number of studies whose participants were athletes showed that increased meal frequency had many benefits. Firstly, it prevents the body from losing lean body mass during a low energy diet. Secondly, it leads to a significant increase in lean body mass and anaerobic power. Thirdly, it helps people get rid of fat.[14][15]
Conclusion
Dividing meals into smaller portions leads to better satiety and allows for better caloric control. However, there are no other proven health benefits linked to this eating pattern. It is thought that the total caloric intake, meal time and the regularity pattern of food intake are important rather than the number of meals per day. Still for some groups of people frequent small meals are beneficial, e.g. for sportsmen it helps to increase the lean body mass and power. So this is the quantity of food and regularity pattern that actually matters the most.
[1] Parks, E., & McCrory, M. (2005). When to eat and how often?. Am J Clin Nutr, 81(1), 3-4. Retrieved from http://ajcn.nutrition.org/content/81/1/3.full
[2] Sierra-Johnson, J., Undén, A., Linestrand, M., Rosell, M., Sjogren, P., & Kolak, M. et al. (2008). Eating Meals Irregularly: A Novel Environmental Risk Factor for the Metabolic Syndrome. Obesity, 16(6), 1302-1307. http://dx.doi.org/10.1038/oby.2008.203
[3] Mattson, M., Allison, D., Fontana, L., Harvie, M., Longo, V., & Malaisse, W. et al. (2014). Meal frequency and timing in health and disease. Proceedings Of The National Academy Of Sciences, 111(47), 16647-16653. http://dx.doi.org/10.1073/pnas.1413965111
[4] Farshchi, H., Taylor, M., & Macdonald, I. (2004). Decreased thermic effect of food after an irregular compared with a regular meal pattern in healthy lean women. International Journal Of Obesity, 28(5), 653-660. http://dx.doi.org/10.1038/sj.ijo.0802616
[5] La Bounty, P., Campbell, B., Wilson, J., Galvan, E., Berardi, J., & Kleiner, S. et al. (2011). International Society of Sports Nutrition position stand: meal frequency. Journal Of The International Society Of Sports Nutrition, 8(1), 4. http://dx.doi.org/10.1186/1550-2783-8-4
[6] Anson, R., Guo, Z., de Cabo, R., Iyun, T., Rios, M., & Hagepanos, A. et al. (2003). Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proceedings Of The National Academy Of Sciences, 100(10), 6216-6220. http://dx.doi.org/10.1073/pnas.1035720100
[7] Horne, B., Muhlestein, J., & Anderson, J. (2015). Health effects of intermittent fasting: hormesis or harm? A systematic review. American Journal Of Clinical Nutrition, 102(2), 464-470. http://dx.doi.org/10.3945/ajcn.115.109553
[8] Hatori, M., Vollmers, C., Zarrinpar, A., DiTacchio, L., Bushong, E., & Gill, S. et al. (2012). Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet. Cell Metabolism, 15(6), 848-860. http://dx.doi.org/10.1016/j.cmet.2012.04.019
[9] Munsters, M., & Saris, W. (2012). Effects of Meal Frequency on Metabolic Profiles and Substrate Partitioning in Lean Healthy Males. Plos ONE, 7(6), e38632. http://dx.doi.org/10.1371/journal.pone.0038632
[10] Bachman, J., & Raynor, H. (2011). Effects of Manipulating Eating Frequency During a Behavioral Weight Loss Intervention: A Pilot Randomized Controlled Trial. Obesity, 20(5), 985-992. http://dx.doi.org/10.1038/oby.2011.360
[11] Kahleova, H., Belinova, L., Malinska, H., Oliyarnyk, O., Trnovska, J., & Skop, V. et al. (2014). Eating two larger meals a day (breakfast and lunch) is more effective than six smaller meals in a reduced-energy regimen for patients with type 2 diabetes: a randomised crossover study. Diabetologia, 57(8), 1552-1560. http://dx.doi.org/10.1007/s00125-014-3253-5
[12] de Castro, J. (2004). The time of day of food intake influences overall intake in humans. J Nutr., 134(1), 104-111. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/14704301
[13] Keim, N., Van Loan, M., Horn, W., Barbieri, T., & Mayclin, P. (1997). Weight Loss is Greater with Consumption of Large Morning Meals and Fat-Free Mass Is Preserved with Large Evening Meals in Women on a Controlled Weight Reduction Regimen. J Nutr., 127(1), 75-82. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9040548
[14] Iwao, S., Mori, K., & Sato, Y. (2008). Effects of meal frequency on body composition during weight control in boxers. Scandinavian Journal Of Medicine & Science In Sports, 6(5), 265-272. http://dx.doi.org/10.1111/j.1600-0838.1996.tb00469.x
[15] Benardot, D., Martin, D., Thompson, W., & Roman, S. (2005). Between-meal Energy Intake Effects On Body Composition, Performance And Total Caloric Consumption In Athletes. Medicine & Science In Sports & Exercise, 37(Supplement), S339. http://dx.doi.org/10.1097/00005768-200505001-01753

The winner of Aug 5th 2018 election is 'Science proves “Leaky Gut” can cause autism (ASD)', please bear with us while our scientist are working hard to deliver the facts for you on this article by Aug 19th 2018

The evidence that omega-3 fatty acids (FAs) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have a cardioprotective effect is increasing, and the American Heart Association recommend consuming at least two servings of fish per week.[1] [2] These cardioprotective benefits can be obtained by eating either farmed and wild fish, with the highest amounts of omega-3 being found in oily fish such as salmon or mackerel. They have been observed from as little as one fish meal per week and improve with every extra meal consumed up to five fish meals per week.[3] One study showed a 29% decrease in mortality in the two year period following a heart attack in patients who were advised to eat oily fish compared to those who were not.[1] In another, where over 18,000 patients with high cholesterol were observed over a five year period, those who were prescribed 1800 mg/day of EPA in addition to statins had significantly fewer coronary events than those prescribed just statins.[4]
Studies have also shown that the mineral and FA content of fish are significantly affected by different cooking methods.[5] [6] One study, for example, concluded that thermal processing of tuna damages the beneficial fats contained within it.[7] In another study, a comparison of cooking methods (baking, frying and microwaving) used to prepare seabass showed that the protein content was significantly changed by all cooking methods and FA levels were generally decreased by most methods.[6] Omega-6 FA levels were shown to increase with frying and omega-3 FA levels increased with microwaving.[6] The conclusion was that to gain the optimum health benefits of FAs from fish, it should be broiled, baked or microwaved, which result in lower levels of less favourable FAs.[5] [6] [8] However, other studies have found that different cooking methods have no effect on omega-3 FA levels. Although in one study fried fish had increased levels of omega-6 FAs and monounsaturated FAs, these were attributed to the oil used for frying.[8]
In addition to effects on FA content, cooking practices can also affect the levels of pollutants, such as heavy metals, present in fish. One study on hammour fish found that, although the majority of the heavy metals present were below maximum permitted levels (MPLs), the levels of lead and arsenic exceeded them.[9] Cooking methods had variable effects on pollutant levels; lead levels decreased with all cooking methods (-16.2% with roasting, -20.7% with frying and -13.2% with broiling), whilst the results for cadmium varied (no change with roasting, totally eliminated with frying and -20.7% with broiling).[9] Freezing the raw fish for six months had no significant effect.[9] Other investigations have found that various cooking methods can affect both the nutrient composition and levels of heavy metal pollutants.[10] The researchers of this study concluded that both excessive frying and the use of salt should be avoided in order to maximise the health benefits of the fish. Furthermore, in order to minimise heavy metal exposure and maximise nutritional benefit, a variety of fish species should be consumed.[10] With regards to mercury levels,a general decrease has been seen with a variety of cooking methods while some mercury can leach out into the water when the fish were boiled.[11]
Baking, boiling and frying fish have been shown to reduce endocrine-disrupting perﬂuorinated compounds (PFCs), for example, baking at 160oC for 15 minutes has been shown to completely remove PFCs.[12] Where radio-caesium was tested, levels appeared increased after deep frying in a study of fish caught on the Savannah River, however this was attributed to the loss of weight from the fish during cooking (i.e.increases in concentration).[13]
In addition to a potential loss of nutrients and alterations in pollutant levels, cancer-promoting substances found in cooked fish are another cause for concern. Carcinogenic heterocyclic amines (HCAs) are produced during various cooking processes. The quantity of HCAs ordinarily consumed is thought to be too low to specifically cause cancer, however, in combination with other mutagens or carcinogens they can be tumour promoters. Hence, it is advisable to minimise HCAs in the diet, for example by microwaving fish instead of frying. It has also been established that supplementing the diet with soy-isoflavones suppresses breast cancer induction by HCAs.[14] Nitrosamines, another group of carcinogenic compounds are also formed during the cooking of fish.[15] This potential for the generation of carcinogenic compounds during cooking is supported by an observed direct association between white fish cooked at high temperatures (pan frying, oven broiling and grilling) and prostate cancer.[16]
However, despite these potential risks, it appears that the health benefits of omega-3 FAs and other nutrients obtained by eating fish may outweigh any associated dangers of cooking FAs rich food. However, care should be taken with the cooking method, temperature, and time. Overall baking and boiling appear to be the safest fish cooking ways. Consuming a variety of species can also decrease the risk of exposure to excessive levels of heavy metals and other pollutants while maximising nutritional benefit.
[1] Burr ML, et al. (1989) Effects of changes in fat, fish, and fibre intakes on death and myocardial re-infarction: diet and re-infarction trial (DART). Lancet, 2, 757–76
[2] Kris-Etherton PM, et al. (2002) Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation, 106, 2747–2757
[3] Psota TL, et al. (2006) Dietary omega-3 fatty acid intake and cardiovascular risk. Am J Cardiol, 98, 3–18
[4] Yokoyama M, et al. (2007) Japan EPA lipid intervention study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet, 369, 1090–1098
[5] Gokoglu N, et al. (2004) Effects of cooking methods on the proximate composition and mineral contents of rainbow trout. Food Chem, 84(1), 19-22
[6] Türkkan AU, et al. (2008) Effects of cooking methods on the proximate composition and fatty acid composition of seabass (Dicentrarchus labrax, Linnaeus, 1758). Food and Bioproducts Processing, 86(3), 163-66
[7] Aubourg S, et al. (1995) A comparison between conventional and fluorescence detection methods of cooking-induced damage to tuna fish lipids. European Food Res Technol, 200(4), 252-55
[8] Neff MR, et al. (2014) Effects of different cooking methods on fatty acid profiles in four freshwater fishes from the Laurentian Great Lakes region. Food Chem, 164, 544-50
[9] Ganbi, HHA. (2010) Heavy metals pollution level in marine hammour fish and the effect of popular cooking methods and freezing process on these pollutants. World J Dairy Food Sci, 5(2), 119-126 [10] Musaiger AO & D’Souza R. (2008) The effects of different methods of cooking on proximate, mineral and heavy metal composition of fish and shrimps consumed in the Arabian Gulf. Arch Latinoam Nutr, 58(1), 103-9
[11] Miero CL, et al. (2016) Fish and mercury: influence of fish fillet culinary practices on human risk. Food Control, 60, 575-81
[12] del Gobbo L, et al. (2008) Cooking decreases observed perfluorinated compound concentrations in fish. J Agric Food Chem, 55(16), 7551-9
[13] Burger J, et al. (2004) Effects of cooking on radiocesium in fish from the Savannah River: exposure differences for the public. Faculty Research & Creative Activity. Paper 60.
[14] Sugimara T, et al. (2004) Heterocyclic amines: mutagens/carcinogens produced during cooking of meat and fish. Cancer Sci, 95(4), 290-99
[15] Huang DP, et al. (1981) Volatile nitrosamines in salt-preserved fish before and after cooking. Food and Cosmetics Toxicology, 19, 167-71
[16] Joshi AD, et al. (2012) Fish intake, cooking practices, and risk of prostate cancer: results from a multi-ethnic case-control study. Cancer Causes Contr, 23(3), 405-20

The winner of Jul 22nd 2018 election is 'How many meals should we eat per day to stay healthy?', please bear with us while our scientist are working hard to deliver the facts for you on this article by Aug 5th 2018

In recent years, the prevalence of asthma and respiratory allergies has increased. The World Health Organisation (WHO) estimates 230 million people now suffer from asthma,[1][2][3] its largest risk factor being the inhalation of substances or particles that cause allergic reactions or irritation of the airways. Common irritants include dust mites, moulds, pet dander and pollen.[4] Contact dermatitis (skin allergy) has also increased, with nickel, latex and chemicals being its main causative agents.[5][6] In Western societies, food allergies have also been on the rise, the most common allergens being milk, eggs, nuts, soy, wheat, fish and shellfish. In fact, it is now estimated that each year at least 30,000 people in the USA require emergency treatment for food allergies, with 150-200 dying as a result.[7] Climate change, environmental pollutants and occupational exposure to specific chemicals also contribute to the development of allergies.[8]
A widely accepted theory termed the ‘hygiene hypothesis’ suggests that the proliferation of allergies is a result of an increasingly ‘hygienic’ world that limits the contact of infant immune systems with microorganisms and bacteria. This could, in theory, prevent them from inducing appropriate responses later in life.[9][10] The theory essentially suggests that our immune systems are no longer challenged in the way they used to be, and thus overreact to allergens that they come into contact with. For example, studies have shown that children who live on farms have a lower incidence of allergy, atopic and non-atopic asthma.[11][12]
The scientific basis of the hygiene hypothesis is related to the balance of two types of white blood cells in our body called T helper 1 and T helper 2 (TH1 and TH2) cells. The balance is changed by bacterial and viral infections, which increase the number of TH1 cells (designed to fight infection) and decrease ‘pro’ allergy TH2 cells (generating allergic response). Whilst this is a widely accepted theory, this hypothesis is now under debate,[13] and it has been contradicted by some studies.[10] One of these studies showed that cleaning the house with bleach did not increase sensitisation to pollen allergens, and in fact, it was shown to protect from the risks of asthma and indoor allergens.[14] To further refute the cleanliness-asthma link hypothesis, other studies found that asthma incidence is decreasing in some Western countries, despite their population is not getting less clean, while in some Latin American countries there are high rates of both infections (due to presumed less cleanliness) and asthma.[12]
The increase in food allergies is thought to originate in changes in diet and increased use of antibiotics, which can both alter the bacterial flora within the gut. This suggestion is supported by the fact that studies have shown a link between the bacteria found in the gut and immune responses including allergy development.[15] [16][17][18] Studies have also shown that the exposure to bisphenol A (BPA) and phthalates – substances commonly found in plastics – during pregnancy and childhood can also cause food allergies. One study found that the concentration of BPA in the urine of pregnant women was directly correlated with wheezing in their children at five years of age, and asthma at three, five and seven years of age.[19] Similarly, higher concentrations of phthalates in pregnant women’s urine have been linked to their children’s allergy risk up to the age of two years of age, even though there was no association with phthalate levels in the children’s urine.[20]
Less predominant risk factors for allergies include genetic ones. For example, children with one allergic parent are more likely to develop an allergy, and there are several genes and polymorphisms associated with asthma or atopy phenotype.[21] Despite that, it is thought that allergy to a specific factor is not hereditary, and the exact mode of inheritance is not yet understood.[22]
Although doubts have been raised over the hygiene hypothesis, avoiding over-cleaning and the non-essential use of antibiotics may still help to reduce the risks of allergies. Being aware of environmental factors is also a way to reduce the risk of allergy development, especially in children. Avoiding products that contain pesticides, phthalates, bisphenols or other toxic substances whenever possible may assist in decreasing the likelihood of developing allergies. Despite the unclear mechanism of allergies inheritance, they may indeed be hereditary, which means that by saving your own health you also save the health of your children.
[1] WHO. (2016) Asthma Retrieved October, 2016, from http://www.who.int/mediacentre/factsheets/fs307/en/
[2] Masoli, M. et al. (2004) The global burden of asthma: executive summary of the GINA Dissemination Committee report. Allergy, 59(5), 469-478.
[3] Bateman ED. et al. (2007) Asthma and allergy - a global perspective. Allergy, 62(3), 213-215.
[4] Silvestri M. et al. (1996) Sensitization to airborne allergens in children with respiratory symptoms. Annals Allergy Asthma & Immunology, 76(3), 239-244.
[5] Kimata, H. (2004) Latex allergy in infants younger than 1 year. Clinical and Experimental Allergy, 34(12), 1910-1915.
[6] Admani S. et al. (2014) Allergic contact dermatitis in children: review of the past decade. Current Allergy and Asthma Reports, 14(4), 421.
[7] FDA. (2016) Food Allergies: Decreasing the Risk. Retrieved 24 October, 2016, from http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm089307.htm
[8] Bush, R., & Peden, D. (2009). Advances in environmental and occupational disorders in 2008. Journal Of Allergy And Clinical Immunology, 123(3), 575-578. http://dx.doi.org/10.1016/j.jaci.2009.01.062
[9] Okada H. et al. (2010) The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update. The Journal of Translational Immunology, 160(1), 1-9.
[10] Brooks, C. et al. (2013) The hygiene hypothesis in allergy and asthma: an update. Current Opinion in Allergy and Clinical Immunology, 13(1), 70-77.
[11] Reidler J. et al. (2000) Austrian children living on a farm have less hay fever, asthma and allergic sensitization. Clinical and Experimental Allergy, 30(2), 194-200.
[12] von Mutius E. et al. (2010) Farm Living: Effects on Childhood Asthma and Allergy. Nature, 10, 861-868.
[13] Yazdanbakhsh, M. et al. (2002) Allergy, parasites, and the hygiene hypothesis. Science, 296(5567), 490-494.
[14] Nickmilder, M., Carbonnelle, S., & Bernard, A. (2007). House cleaning with chlorine bleach and the risks of allergic and respiratory diseases in children. Pediatric Allergy And Immunology, 18(1), 27-35. http://dx.doi.org/10.1111/j.1399-3038.2006.00487.x
[15] Frei, R. et al. (2012) Microbiota and dietary interactions – an update to the hygiene hypothesis? Allergy, 67(4), 451-461.
[16] Maslowski, KM. et al. (2011) Diet, gut microbiota and immune responses. Nature, 12, 5-9.
[17] Stefka, AT. et al. (2014) Commensal bacteria protect against food allergen sensitization. Proceedings of the National Academy of Sciences of the USA, 111(13145-13150).
[18] Berni Canani, R. et al. (2015) The role of the commensal microbiota in the regulation of tolerance to dietary allergens. Current Opinion in Allergy and Clinical Immunology,15(3), 243-249.
[19] Donohue, KM. et al. (2013) Prenatal and postnatal bisphenol A exposure and asthma development among inner-city children. Journal of Allergy and Clinical Immunology,131(3), 736-742.
[20] Stelmach, I. et al. (2015) The effect of prenatal exposure to phthalates on food allergy and early eczema in inner-city children. Allergy and Asthma Proceedings, 36(4), 72-78.
[21] Vercelli, D. (2008). Discovering susceptibility genes for asthma and allergy. Nature Reviews Immunology, 8(3), 169-182. http://dx.doi.org/10.1038/nri2257
[22] Los, H., Postmus, P. E., & Boomsma, D. I. (2001). Asthma Genetics and Intermediate Phenotypes: A Review From Twin Studies. Twin Research, 4(2), 81–93. http://doi.org/10.1375/twin.4.2.81

The winner of Jul 8th 2018 election is 'What fish cooking method is the healthiest', please bear with us while our scientist are working hard to deliver the facts for you on this article by Jul 22nd 2018

Since plastics were first produced in the early 1900s, they have become ubiquitous in our daily lives. The term “plastic” covers an array of organic and inorganic compounds. Substances, known as plasticisers, are often added to the raw ingredients to shape or stabilise plastics. To manufacture clear hard plastic, a chemical called bisphenol A (BPA) or its alternatives bisphenol S (BPS) or bisphenol F (BPF) are often utilised.[1] [2] For soft, flexible plastic, however, phthalates are often used.[3]
All of these substances are known to be harmful endocrine disrupting chemicals (EDCs).[4] [5] [6] EDCs can affect the body’s development, growth and hormone balance by mimicking, blocking or otherwise disrupting the body’s natural hormones.[7] [8] Unborn and young children seem to be more susceptible; for example EDC exposure during early foetal development increases the probability of negative health outcomes later in life, including cancers, neurodevelopmental and neurodegenerative diseases, metabolic disorders, asthma and immune disorders.[9]
It is an unfortunate fact that these toxic chemicals can leach from plastic containers into food. Worse still, many of the actions that we do to food containers can increase the level of migration of the toxic chemicals. Exposing plastic to heat by processes such as washing at high temperatures, microwaving or adding hot food or liquid can increase the leaching of chemicals into the contents, as can mechanical stress and exposure to sunlight. Furthermore, toxin migration is likely to be greater when plastic comes into contact with fatty foods such as meat or cheese.[10]
BPA is proven dangerous, and the use of BPA in the manufacture of baby bottles has now been prohibited in the USA and the EU. However it is often replaced with BPS or BPF, which are currently still authorised for use in baby bottles, despite them causing many of the same harmful effects as BPA.[11] This means that even products marketed as “BPA-free” can still be dangerous to use, as its toxic alternatives (BPS or BPF) are still commonly found in baby bottles, other food containers and all other plastic goods. These other food-contact goods, especially reusable bottles used during sports, are often left in the car or carried around in warm weather, where increased temperatures increase the risk of contamination by leached toxic chemicals.[12] The type and amount of chemical that leaches into the food or drink depends on numerous factors, including the type of plastic, the time for which it is heated, and the condition of the plastic container.[13] However it is not just through our food that we are exposed to these toxic EDCs; in the case of polybrominated diphenyl ethers (PBDEs) we are also exposed via dust inhalation and our household furniture, our car upholstery and even our electronic devices.[14]
Testing of chemical migration from plastic does form part of the legislation regarding the use of plastic containers for storing food, however regulations are potentially not stringent enough to protect us fully, as they do not account for cumulative exposures or multiple exposure routes in our households. Testing involves measuring the quantity of chemicals that leach into the food during “normal use”.[15] However, when the overall migration is below the limit considered safe by the relevant regulatory body, risk assessments on specific harmful substances may not be carried out. Worse still, testing measures the quantities of toxins leaching into one serving of food, without taking into consideration the frequency at which an individual is exposed to these toxins, or the multiple routes through which they may be exposed. Exposure can be high when plastic containers are used frequently, or when the individual is exposed to toxic chemicals from a range of sources in addition to food, such as widespread exposure to PBDEs in a variety of household products, including dust.[14]
Given the potential for such dangerous contamination of our food from plastic containers, the best choice for food storage and heating may therefore be to use safer alternatives. While some plastics may claim to be a ‘safer’ alternative, such as products marketed as “BPA-free”, they may still leach harmful chemicals such as EDCs into food and drink, as toxic BPA has simply been replaced with equally dangerous BPS and BPF. In fact these chemicals may actually be more dangerous, as they have shown the potential for even greater EDC activity.[16] This bending of the rules by manufacturers, coupled with poor regulation, mean that plastic alternatives, such as glass, are the safer option to limit your toxin exposure. But be sure to check the seal of your glass container lids though - these are often made using potentially toxic plastics additives too.
[1] Halden, RU. (2010) Plastics and health risks. Ann Rev Pub Health. 31. 179-194.
[2] Viñas, R. & Watson, CS. (2013) Bisphenol S disrupts estradiol-induced nongenomic signaling in a rat pituitary cell line: effects on cell functions. Environ Health Perspect. 121(3). 352-8.
[3] Shen, H-Y. (2005) Simultaneous screening and determination eight phthalates in plastic products for food use by sonication-assisted extraction/GC–MS methods. Talanta. 66(3). 734-9.
[4] Mersha, MD. et al. (2015) Effects of BPA and BPS exposure limited to early embryogenesis persist to impair non-associative learning in adults. Behav Brain Funct. [epub ahead of print] doi: 10.1186/s12993-015-0071-y
[5] Qiu, W. et al. (2016) Actions of Bisphenol A and Bisphenol S on the Reproductive Neuroendocrine System During Early Development in Zebrafish. Endocrinology. 157(2). 636-47.
[6] Sheikh, IA. et al. (2016) Endocrine Disruption: Computational Perspectives on Human Sex Hormone-Binding Globulin and Phthalate Plasticizers. PLoS One. 11(3). [epub ahead of print] doi: 10.1371/journal.pone.0151444.
[7] Casals-Casas, C. & Desvergne, B. (2011) Endocrine disruptors: from endocrine to metabolic disruption. Ann Rev Physiol. 73. 135-62.
[8] Roy, J. et al. (2009) Estrogen-like endocrine disrupting chemicals affecting puberty in humans--a review. Med Sci Monit. 15(6). RA137-45.
[9] Landrigan, P. et al. (2003) Assessing the effects of endocrine disruptors in the National Children's Study. Environ Health Perspect. 111(13). 1678-82.
[10] Munguía-López, EM. et al. (2005) Migration of bisphenol A (BPA) from can coatings into a fatty-food simulant and tunafish. Food Addit Contam. 22(9). 892-8.
[11] Eladak, S et al. (2015) A new chapter in the bisphenol A story: bisphenol S and bisphenol F are not safe alternatives to this compound. Fertil Steril. 103(1). 11-21.
[12] Greifenstein, M. et al.(2013) Impact of temperature and storage duration on the chemical and odor quality of military packaged water in polyethylene terephthalate bottles. Sci Total Environ. 456-7. 376-83.
[13] Cooper, JE. et al. (2011) Assessment of bisphenol A released from reusable plastic, aluminium and stainless steel water bottles. Chemosphere. 85(6). 943-7.
[14] Imm, P. et al. (2009) Household exposures to polybrominated diphenyl ethers (PBDEs) in a Wisconsin cohort. Environ Health Perspect. 117(12). 1890-5.
[15] Intertek. (2016) European Union Food Packaging and Materials Migration Testing. Retrieved April 2016 from, http://www.intertek.com/packaging/testing/food-migration/
[16] Chen, D. et al. (2016) Bisphenol Analogues Other Than BPA: Environmental Occurrence, Human Exposure, and Toxicity - A Review. Environ Health Perspect. 50(11). 5438-53.